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PubMed1980

[Genetic variability of colonies of noninbred Cubavet and CENIC laboratory mice from the Republic of Cuba].

Genetic structure of non-inbred Cubavet and CENIC mice colonies was investigated for three loci of hair colouring (A, B, D), for potential fertility and embryo mortality. Mice colonies are polymorphis in three hair colour determining loci. Alleles rates are: a -- 0.17--0.36; b -- 0.21--0.26; d -- 0.07--0.17. Both colonies reliably differ in colour genotype distribution (p less than 0.001). There are also some differences in the number of live embryos, yellow bodies and postimplantation mortality (p less than 0.05--0.001). The data obtained allow to control the stability of genetic structure of the population for a long time.

Alleles↗
PubMedDate not supplied

Production and reproductive performance of hexaparental and octaparental mice.

The production of hexaparental and octaparental mice following embryo aggregation is reported. These mice were progeny-tested to determine which cell components were contributing to gamete formation. One chimera (No. 15) was shown to be producing eggs from all three cell strains--white, yellow, and black. The other chimeras tested were not forming germ cells from all of the cell strains involved. The use of these animals for obtaining a minimum estimate of the number of cells giving rise to the embryo proper is discussed. The suggestion is made that multi-embryo aggregates may actually be developmentally different from normal sized embryos and this may result in modified mechanisms of cell recruitment.

Animals↗
PubMed1980

[Ethnic variation in congenital pigmentation anomalies].

Clear ethnic differences are observed in the major form of tyrosinase-negative oculocutaneous albinism as well as in other forms of oculocutaneous albinism, cutaneous albinism and the very rare ocular albinism. Most interesting is the borderline between normal variation and abnormal forms, especially illuminated in rutilism or red headedness in Negroids and high frequencies of pigmentation anomalies without appreciable disadvantages for the carrier, e.g., the reddish skin of geographically isolated Papuans. The very differential frequencies of the occurrence of pigmentation anomalies in some populations are influenced as well by population genetic factors (isolation/inbreeding, founder-effect, heterosis) as also by socio-cultural factors (albinism as a marriage barrier, infanticide), and in some areas perhaps some kind of negative selection in which individuals with the character in question fail to reach reproductive age.

Adolescent↗
PubMed1994

Instability at the W/c-kit locus in mice: analysis of melanocyte cell lines derived from reversion spots.

Mutations at the mouse W/c-kit locus have pleiotropic defects including impaired development of the melanocyte lineage. We have characterized the molecular basis of the Wei mutation. We show here that Wei is the result of a missense mutation in the ATP binding site domain of c-kit proto-oncogene which affects the tyrosine kinase function of the receptor. As a result, few melanoblasts survive during embryogenesis in heterozygous Wei/+ foetuses. Therefore the adult skin is partly devoid of differentiated pigmented cells giving rise to a mottled coat colour phenotype. However, three per cent of Wei/+ mice exhibit spots of wild-type pigmentation on the coat which is otherwise of mutant phenotype. Such areas are known as phenotypic reversions. To dissect the molecular events responsible for the phenotypic instability of the Wei mutation, we have isolated pure cultures of continuously proliferating melanocytes from two independent reversion spots. These melanocyte lines, designated Wei-R1 and Wei-R2, were shown to exhibit none of the characteristics associated with transformed melanocytes. We have used a polymorphic restriction site generated by the Wei mutation to show that both melanocyte lines are still heterozygous at the W focus. Furthermore, Wei-R1 and Wei-R2 melanocytes express both the mutated and the wild-type c-kit RNA. These results indicate that the somatic mutation events responsible for reversion spots are not necessarily associated with loss of heterozygosity at the W/c-kit locus. Together with previous data, this points to the fact that several mechanisms account for the coat colour reversion phenotype.

Alleles↗
PubMed1995

Tyrosinase inhibition due to interaction of homocyst(e)ine with copper: the mechanism for reversible hypopigmentation in homocystinuria due to cystathionine beta-synthase deficiency.

Deficiency of cystathionine beta-synthase (CBS) is a genetic disorder of transsulfuration resulting in elevated plasma homocyst(e)ine and methionine and decreased cysteine. Affected patients have multisystem involvement, which may include light skin and hair. Reversible hypopigmentation in treated homocystinuric patients has been infrequently reported, and the mechanism is undefined. Two CBS-deficient homocystinuric patients manifested darkening of their hypopigmented hair following treatment that decreased plasma homocyst(e)ine. We hypothesized that homocyst(e)ine inhibits tyrosinase, the major pigment enzyme. The activity of tyrosinase extracted from pigmented human melanoma cells (MNT-1) that were grown in the presence of homocysteine was reduced in comparison to that extracted from cells grown without homocysteine. Copper sulfate restored homocyst(e)ine-inhibited tyrosinase activity when added to the culture cell media at a proportion of 1.25 mol of copper sulfate per 1 mol of DL-homocysteine. Holo-tyrosinase activity was inhibited by adding DL-homocysteine to the assay reaction mixture, and the addition of copper sulfate to the reaction mixture prevented this inhibition. Other tested compounds, L-cystine and betaine did not affect tyrosinase activity. Our data suggest that reversible hypopigmentation in homocystinuria is the result of tyrosinase inhibition by homocyst(e)ine and that the probable mechanism of this inhibition is the interaction of homocyst(e)ine with copper at the active site of tyrosinase.

Adolescent↗
PubMed1995

[A study of autogenous hair transplantation in Chinese].

From Sep. 1988 to Dec. 1992, a total of 980 procedures of autogenous punch grafts were performed in 395 patients with alopecia. This technique has mainly been used for seborrheic alopecia and cicatricial alopecia with sufficient hair in the donor site. Chinese people are unfavorably characterized by one-third less amount of hair than Westerners, lank hair shaft and strong contrast of color between the hair and hair-bearing scalp. The technique of L shape punch grafts was used for patients with insufficient hair in the donor site. Insertion of mini-grafts between the anterior rows of punch grafts made the frontal hairline more natural in appearance and eliminated the necessity of postoperative scalp tattoo. The results were perfect. We concluded that adult alopecic patients are good candidates for punch graft procedure, and for children and juvenile patients, scalp expansion is preferable.

Adolescent↗
PubMed1993

Mast cell number in the skin of heterozygotes reflects the molecular nature of c-kit mutation.

The W locus of mice encodes the c-kit receptor tyrosine kinase. Heterozygous WJic/+ and Wn/+ mice and homozygous Wf/Wf mice were similar in appearance; all of them have large depigmented areas lacking any well-defined pattern. The WJic, Wn, and Wf mutant alleles were characterized and their molecular nature was correlated with the mast cell differentiation in the skin and the biologic features of cultured mast cell (CMC). All WJic, Wn, and Wf were point mutations at the tyrosine kinase domain, and c-kit mRNA was normally transcribed from all of them. The mature 145-Kd form of the c-kit protein was produced from the WJic and Wf alleles, but not from the Wn allele. c-kit proteins produced by the WJic or Wf allele were expressed on the surface of CMCs, but those of the Wn allele were not. When double heterozygous mice were produced between W and WJic and between W and Wn, both W/WJic and W/Wn mice lacked skin mast cells. W/WJic CMCs and W/Wn CMCs did not survive in the coculture with fibroblasts. W/WJic CMCs normally attached to fibroblasts, but W/Wn CMCs did not. The defect of W/Wn CMCs in the attachment was attributed to the deficient extracellular expression of the c-kit protein. The number of skin mast cells was compared among WJic/+, Wn/+, Wf/+, and Wf/Wf mice. Mast cells decreased in WJic/+ and Wf/Wf mice, but not in Wn/+ and Wf/+ mice. Although the Wn was a point mutation at the kinase domain, the biologic effect of the Wn was comparable with that of the W mutant allele, which produces truncated c-kit protein without the transmembrane domain. The weak phenotype of Wn/+ mice may be explained by the deficient extracellular expression of c-kit proteins produced by the Wn allele. When WJic/WJic, Wn/Wn, and Wf/Wf CMCs were stimulated by the recombinant c-kit ligand, autophosphorylation activity was observed only in Wf/Wf CMCs. This result was consistent with the weak biologic effect of the Wf mutant allele.

Adenosine Triphosphate↗
PubMed1995

Inherited thrombocytopenia caused by reduced platelet production in mice with the gunmetal pigment gene mutation.

Hereditary macrothrombocytopenia and prolonged bleeding times are associated with the recessive mouse pigment dilution gene gunmetal (gm). Other platelet abnormalities include a mild storage pool deficiency and abnormal expression of two low-molecular-weight guanosine triphosphate binding proteins. These studies were designed to further elucidate the cause of the macrothrombocytopenia. The life span of gunmetal mouse platelets was not significantly different from normal. However, rates of platelet synthesis, measured by sulfate incorporation, were decreased to 25% of normal values. Bone marrow transplantation of normal marrow cells corrected the thrombocytopenia. Furthermore, direct morphologic analysis of mature mutant marrow megakaryocytes by transmission electron microscopy showed reductions in the normal cytoplasmic demarcation membrane system, areas of abnormal membrane complexes, and an increased incidence of emperipolesis. Mutant platelets were relatively more heterogeneous in size and contained unusual elongated and striated inclusions. Mutant megakaryocyte numbers were increased threefold to fivefold over normal numbers in marrow and spleen. Thus, the efficiency of platelet production from gunmetal megakaryocytes is reduced by an order of magnitude. Mutant marrow had a greater proportion of 32N and a smaller proportion of 8N megakaryocytes. Collectively, the results indicate that the gunmetal gene acts intrinsically in megakaryocytes and that an abnormality in this gene causes significant qualitative and quantitative effects on platelet production.

Animals↗
PubMed1995

Nicotine and cotinine accumulation in pigmented and unpigmented rat hair.

This study was performed to assess the contribution of systemic and external uptake to nicotine accumulation in hair. The systemic nicotine uptake in hair was determined in pigmented rats (Brown Norway) and albino rats (Sprague-Dawley) after subcutaneous administration of 3 doses of nicotine with osmotic minipumps [5, 10, and 20 mg/(kg x day) for 3 weeks], the highest dose also following metabolic enzyme induction. The external nicotine uptake was determined in cut hair of both strains after exposure to room-aged cigarette sidestream smoke, a surrogate for environmental tobacco smoke (nicotine concentration: 5 micrograms/liter for 1, 2, and 3 weeks). Nicotine and its metabolite cotinine were determined using capillary GC after complete alkaline digestion of the hair sample and solvent extraction. Systemic uptake: Nicotine and cotinine concentrations in hair were dose-dependent and correlated with plasma concentrations. The nicotine concentration was approximately 20 times higher in pigmented than in unpigmented hair. The cotinine concentration was approximately 10 times lower than the nicotine concentration in pigmented hair. After enzyme induction before administration, nicotine and cotinine concentrations in hair were significantly reduced in parallel to the reduced plasma concentrations, showing the influence of metabolism. External uptake: Nicotine was found in the hair of both strains, the concentration in pigmented hair being a factor of 1.5 higher than in unpigmented hair. Thus, hair pigmentation had a major influence on systemic uptake in hair and a minor influence on external uptake in hair.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

[Age estimation by appearance of gray hair in pubic hair].

The pubic hair of Japanese males aged 12-90 years old (n = 123) and females 14-85 ys. (n = 80) autopsied during 1984-1993 was investigated to determine its appearance age and possible appearance age of gray hair. As the appearance degree of gray hair in pubic hair 5 stages were applied to samples to establish a criterion for age estimation. Stage 0; no gray hair, 1; 1-3 gray hairs, 2; a few-10, 3; 10 gray hairs-2/3 of the entire pubic hair, 4; more than 3/4. The appearance age of gray hair with appearance rate 100% (75%) was more than 65 (55) ys. in both sex. The possible appearance age was more than 30 ys. in males and 36 ys. in females, practically younger than "45 years old" which had been described in texts. The age range with a hit rate 100% is at stage 0; less than 62 ys. in males, less than 59 ys. in females, at stage 1; 30-64 ys. in males, 36-60 ys. in females, at stage 2; 43-72 ys., 39-85 ys. and at stage 3; 49-77 ys,--.

Adolescent↗
PubMed1995

bcl-2 deficiency in mice leads to pleiotropic abnormalities: accelerated lymphoid cell death in thymus and spleen, polycystic kidney, hair hypopigmentation, and distorted small intestine.

Transgenic mice homozygously lacking in the bcl-2 gene were generated using homologous recombination in embryonal stem cells. The complete absence of Bcl-2 alpha and -beta proteins did not interfere with normal embryonic development. Abnormalities became evident after birth, although the severity varied among homozygous null mice, bcl-2-/- mice displayed pleiotropic abnormalities similar to those in the previously described bcl-2-/- mice, including growth retardation, smaller ears, short lives, polycystic kidney, atrophic thymus and spleen with accelerated apoptotic cell death of lymphocytes, and hair hypopigmentation in the second hair follicle cycle. Our bcl-2-/- mice also revealed novel defects in the small intestine, characterized by retarded development, accelerated exfoliation of epithelial cells, and very few mitotic progenitor cells.

Abnormalities, Multiple↗
PubMedDate not supplied

[The characteristics of the accumulation of metals in the hair of children].

Gender- and colour-associated quantitative features of accumulation of zinc, copper, nickel, lead, molybdenum and chromium have been studied in the hair of children aged 3-4 yr residing in different districts of Kiev. Inverse relationship was found between accumulation of lead and zinc, zinc and copper; direct proportionality between copper and lead, chromium and molibdenum. The levels of nickel detected in 34% of the hair samples did not permit establishing the pattern of this metal relations to other metallic elements.

Child, Preschool↗
PubMed1994

Genetic characterization of the mouse strains of the Institute for Animal Breeding of the Veterinary Faculty of the University of Munich, Germany.

A total of 15 strains of mice (11 inbred lines, 4 outbred stocks) of the institute for animal breeding of the veterinary faculty of the university of Munich (FRG) were scored for 23 biochemical loci each. The allelic distribution and frequencies were recorded as a basis for a so far not established genetic monitoring system. The inbred strains revealed the expected homozygosity with one exception (strain UMDH/+; locus Es1). The outbred stocks showed a remarkable degree of variable loci (17.4-36.3%) with a mean heterozygosity between 0.05 and 0.12. The markers in use allow differentiation between all strains (except for one pair of sublines) and stocks. 14 of the loci show allelic differences among the strains and thus can be used for a genetic monitoring system.

Alleles↗
PubMed1994

The Pmel 17/silver locus protein. Characterization and investigation of its melanogenic function.

The silver mutation in mice causes progressive graying of hair due to the loss of functional follicular melanocytes. Recently the silver locus gene (called Pmel 17) has been cloned; its encoded product shares homology with a chick melanosomal matrix protein and a bovine retinal pigment epithelial protein. Although the sequence of the silver gene and the correlation of its expression with pigment production have been reported, its function in melanogenesis is still unknown. In an effort to characterize that function, we have synthesized the predicted carboxyl-terminal peptide of the mouse Pmel 17 protein and generated a rabbit polyclonal antibody (alpha PEP13) to it; that antibody recognized the silver protein specifically. The immunoaffinity-purified silver protein lacked all of the known melanogenic catalytic activities which other tyrosinase-related proteins (TRP) have, nor did it appear to modulate any of those TRP activities. Metabolic labeling experiments demonstrated that the silver protein disappears in vivo within a few hours, indicating that it is rapidly degraded, or quickly processed to lose its carboxyl terminus. Cross-reactivity experiments showed that a recently reported anti-melanosomal matrix protein antibody (alpha MX) also recognizes the silver protein, although at a different epitope from that of alpha PEP13. Using Western immunoblotting, we analyzed subcellular fractions isolated from B16 F10 melanoma cells and found that the silver protein was rich in the melanosome fraction but was absent from coated vesicles which deliver TRPs to melanosomes. These results suggest that the silver locus product is a melanosomal matrix protein which may contribute to melanogenesis as a structural protein, although the possibility remains that it also has a novel catalytic function in melanogenesis.

Amino Acid Sequence↗
PubMed1994

Accelerated deaths from systemic lupus erythematosus in NZB x NZW F1 mice treated with the testosterone-blocking drug flutamide.

In the New Zealand black (NZB) x New Zealand white (NZW) (B/W) mouse model of systemic lupus erythematosus (SLE), females die prematurely and males have late onset of disease. It has been proposed that testosterone protects B/W mice from rapidly progressive SLE. The mechanisms of androgenic suppression of the immune system, however, are not understood. We tested the hypothesis that testosterone exerts protective effects in males through classic receptor-mediated actions. Flutamide, a potent and specific androgen receptor blocker, was administered continuously to B/W mice from 6 weeks of age, and the animals were monitored in a longevity study. Our supposition that flutamide treatment would accelerate disease was upheld in female B/W mice. In females, flutamide clearly accelerated mortality and reduced longevity to (median) 30 weeks as compared with 37 weeks in controls (p = 0.003). In male B/W mice, mortality was identical in treated and control animals in the early phase of the study, and deleterious effects of treatment were apparent only after the first year of treatment. Flutamide-treated males had significant elevation of serum testosterone, but their atrophied seminal vesicles strongly suggested that peripheral androgen effects were blocked. Albuminuria, blood urea nitrogen, and anti-DNA antibodies were not altered by flutamide in females or males. The receptor-mediated effects of androgens on murine autoimmune disease were dependent on gender and were noted primarily in females and in males that survived past 1 year of age.

Albuminuria↗